Myofascial Genesis of Unpleasant Thoughts and Emotions

It is common for patients who are laden with chronic, intense myofascial constrictions to report severe mental agitation, fretting, insomnia, and other unpleasant thoughts and emotions. It is also common to hear these patients exclaim how profoundly relieved they are of their unpleasant thoughts and emotions after therapy relieves their constrictions and associated trigger points.

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In the typical chiropractic office, both the doctor's and the patient's attention are usually on physical pain, and it's easy for the doctor to overlook the relation of the physical pain to the patient's emotional suffering. Even when a patient makes it clear that his emotions are being adversely affected by his physical pain, the doctor may be hesitant to deal with the patient's disturbed emotions. The doctor may feel, for example, that lengthy counseling may be needed and that this is incompatible with the time constraints of a chiropractic practice.

Unless the doctor has had special training in psychotherapy, it is probably best that he leave that form of treatment to clinicians who specialize in it. Giving encouragement, emotional support and practical advice is possibly the limit of what the typical doctor can reasonably provide in the way of psychological care. Fortunately, though, a great deal of patients' unpleasant thoughts and emotions are based on the state of their myofascial tissues; and the appropriate therapy is not psychotherapy but treatment of this physical conditions.

If the client's emotional condition is of myofascial origin, the quickest, most effective, and most reliable way to give him thorough relief is through treatment directed to his myofascia.[1]

Myofascial Receptors

Pain motivates most patients with myofascial constrictions and trigger points to seek clinical care. Receptors that give rise to the perception of pain are housed in the myofascia, and sustained myofascial constrictions and their trigger points tend to activate these receptors. Presumably, the adequate stimulus for the pain is an event in the myofascia that threatens or causes tissue damage.[2] Constrictions may cause tissue damage by compressing the arteries, veins and lymphatic nodes that course through the constricted myofascia.

Factors that Induce Fibrosis of Fascial Tissues

Traditionally, fascial tissue wasn’t given as much attention as muscle by researchers and clinicians. This began to change in the early 1980s. From that time, a variety of practitioners have stimulated a great deal of interest in fascia. For the most part, the practitioners who’ve done so have been massage therapists and myofascial trigger point therapists. However, some physical therapists and osteopathic, medical, and chiropractic physicians have also made notable contributions.

Health care consumers because myofascial practitioners have provided relief from pain and dysfunction that result from abnormalities of fascial tissues.

Dr. Ida Rolf first began to promote her view in the 1950's that fascial tissues bind muscles and thereby impede adaptive, fluid motion of the body.

Dr. Ray Nimmo, the chiropractor who championed trigger point therapy in the middle of the 20th century, didn't agree with her: ‘I could not agree,’ he wrote, ‘with her explanation that the muscles were bound down by connective tissue and had to be broken loose. Connective tissue is too strong to be broken loose.’ .. What it was, of course, was tensed musculature.’

Today we have data that show Ida Rolf was right. Fascia does bind together, and it can be broken loose. Most of these data come from studies of either connective tissue injury or peripheral joint stiffness after periods of immobility.

These studies aren't tantamount in depth nor breadth to the advanced and voluminous research that's been done on muscle. However, they do show that the fascia can contribute in at least three ways to the conditions experienced by the myofascial patient.

Three main factors that result in fascial abnormalities.

Trauma
Chronic strain
Immobility of fascial tissues.

It can do this by becoming fibrotic when traumatized or when subjected to chronic strain. It can also do so by webbing together after periods of immobility. Any of these conditions can restrict mobility and pull myofascial attachments. The pulling can cause compression that impedes blood flow, produces energy-deficient contractures and trigger points, and sets off adverse neurological ramifications.

Trauma to Fascia

When fascia has been traumatized, it heals with a special type of collagen fiber called type III. These collagen fibers are laid down irregularly in all different directions. As the inflammation heals, the collagen fibers web the breach together. Applying cross-friction massage as the inflammation is resolving may help orient the fibers in a linear direction, with the stress lines of the tissue that's healing. If the fibers do become oriented to the stress lines, this may leave the body part normally mobile after the healing process is completed.

If the fibers are allowed to remain irregularly webbed, however, they’ll contract and draw the tissue together toward its center. The contracted fibers will reduce the mobility of the myofascial tissue they’re attached to. As the collagen fibers shorten, the pressure within the myofascial tissue will increase. The increased pressure will compress the arteries, veins, and lymphatics that course through the contracting tissue. This will create ischemia and, again, will induce energy-deficient contractures and trigger points.

Chronic Strain on Fascial Tissue.

When fascia is chronically overloaded, myofascial pain syndromes can be exceedingly difficult to relieve. Chronic intermittent tension-loads on a myofascial tissue stimulates fibroblasts within the fascia to produce more collagen. Collagen therefore accumulates in the overloaded tissue. Fibrous tissue adapting this way to a mechanical load imposed on it is known as the "stretch-hypertrophy rule."

Most myofascial practitioners have palpated the effect of this stretch-hypertrophy. They’ve done so when they’ve palpated the hard, fibrous cords that run longitudinally along each side of the thoracic spine in the erector spinae muscles. Some practitioners call these cords "linear fibrosis." The fibrosis is especially prominent in the patient who projects his head out in front of the gravity line, as though leading his body with it when he walks. The upper thoracic erectors have to guy-wire the patient's head and neck---sometimes more, other times less. And this intermittent overloading stimulates the fibroblasts to synthesize and deposit so much collagen in the fascial layers that the erector muscles in some patients feel like steel cables.

I've found referring trigger points in these muscles in many patients. The trigger points are usually highly resistant to specific myofascial therapy. The treatment resistance suggests that the trigger points aren't just in contractured muscle. Contractured muscle is usually capable of releasing its tension, elongating, and thereby allowing inactivation of the trigger point. The treatment resistance of the trigger points instead implies that fibrous (or what some call "dystrophic") tissue is involved.

Immobility

When fascia remains immobile for a time, perhaps as little as four weeks, cross-bindings can form between the molecules of its type I collagen. Type I is the normal collagen constituent of connective tissues. These cross-bindings reduce the flexibility of the fascia. They do this, at least in part, by restricting gliding between fascial sheets.

When connective tissue stays immobile, changes in the ground substance are perhaps more clinically important than the effects on collagen fibers. Protein-carbohydrate complexes in the ground substance bind water and give it its amorphous gel quality. (Researchers formerly called these water-binding complexes mucopolysaccharides, but they’ve changed the name to glycosaminoglycans.)

With immobility, the complexes gradually disappear from the ground substance. As a result, progressively less water is bound, and the bulk of the ground substance diminishes. As this happens, the collagen fibers come closer together. When the distance from one collagen molecule to another diminishes beyond some critical threshold, the molecules begin forming cross-bindings. As more and more molecules cross-bind, the involved connective tissue become less and less elastic. The tissue becomes less elastic because the collagen fibers and fascial sheets lose the ability to slide freely along one another. The effect is as though the tissue has lost some lubricating factor. But it appears that the collagen molecules of fascial sheets are actually tethered together.

Reduced mobility, or virtually immobility, of myofascial tissues is part of the problem with the patient who has heavy fibrosis of the upper thoracic erector spinae myofascia. Sustained guide wiring of a forward-projecting head and neck chronically overloads these paraspinal myofascial tissues. This stimulates fibrosis. To worsen the problem, the upper thoracic spine has minimal mobility compared to the spine in the lower thoracic, lumbar, and cervical areas. And unless a person works at it, the paraspinal myofascia in the upper thoracic area is seldom stretched, torqued, or laterally bent. It just sits there. As fibroblasts deposit more and more collagen in response to the guy-wiring, the collagen appears to cross-link to form the thick cords we myofascial practitioners are so familiar with.

Latent Trigger Points in the Elderly

Most of us myofascial practitioners have patients who keep some—maybe even most—of their body parts practically immobile. That is, they use certain parts of their bodies in a guarded, tightly restricted range of motion. This is especially true of elderly patients. Many of these people have trigger points in these relatively immobile tissues, although most of the trigger points are "latent." This means, of course, that the trigger points aren’t actively referring pain.

Travell and Simons (the authors of the famous Trigger Point Manuals) have pointed out that many elderly people have latent trigger points. They say these people seem to automatically restrict their range of motion to avoid activating and suffering from their trigger points. Based on this principle, these elderly people’s myofascial tissues are more likely to be fibrotic. This is likely because their reduced mobility permits type I collagen fibers to cross-link extensively throughout their bodies.

The cross-linked collagen will exhibit physiological creep—that is, a steady pulling in on itself. At some critical point, the creep will cause the pressure within the tissues to increase to a critical point. At this point, blood flow will diminished, perhaps to the level of ischemia, and pain-mediating mechanoreceptors will be activated. At this time, the people will begin experiencing pain although they restricted their motion to avoid it. This is consistent with the view that the amount of collagen in connective tissues increases with age, making old animal meat tough. While the amount of collagen increases, the collagen fibers also develop extensive type I cross-linking.

As the years pass, many people restrict their body movements more and more. Eventually, their capacity for mobility becomes markedly reduced and they generally perceive stiffness. Mobility is important to tissue fluid exchange, and so their limited mobility seriously reduces blood flow. Blood flow in some circumscribed areas becomes so sluggish that the tissues become distinctly ischemic.

At that stage, real trouble begins. First, energy-deficiency contractures can form and create trigger points. Far worse, though, the ischemia can cause muscle fibers to deteriorate. At the same time, fibroblasts become active and increase their output of collagen, bringing about some degree of myofascial fibrosis. The collagen fibers of this fibrotic area are likely to form cross-bonds that will tighten the tissue even more.

If the receptors of type C and type A delta nerves are trapped in this squeezing fibrotic tissue, the patient is likely to experience local tenderness and referred pain. These nerve responses are also likely to facilitate the segments of the spinal cord they enter. (Facilitation refers to a lowered threshold for neuronal firing.) This will stimulate motor fibers at the same level and cause hypertonicity of the associated paraspinal muscles. The nerve signals will also ascend to the brain stem and stimulate their reticular activating formations. The signals will also reach the thalamus. From there, relayed signals will stimulate cortical centers, disturbing thought and perception. The signals will also reach the basal (limbic) areas of the brain beneath the thalamus, which can produce disturbed emotions and interfere with the body's general homeostasis.

When relatively immobile myofascia lead to pain, freeing the patient from it may be difficult. Patients with fibrotic tissue aren't as responsive to therapy as patients whose source of pain is muscle contractures. There are at least two reasons for this.

First, fibrotic tissue can only be softened or stretched, and its cross-binds broken. First, in between therapy sessions, the tissue can shorten again unless the patient works diligently to keep it elastic. Diligence is required to counter the "physiological creep" I mentioned before. Second, many people who’ve minimized their movements to avoid myofascial pain have lost mobility and become generally stiff. They may lack the flexibility to cooperate in stretching muscles that house painful contractures and trigger points. For some of these people, relief can come only from therapies such as ultrasound and cross-friction massage that soften fibrotic tissues. Stretching the involved tissues, however, is fundamental to long-term improvement. If the patient isn’t able to effectively stretch because of severe inflexibility, he may require clinical care at frequent intervals.

Dr. John C. Lowe